Genetic variation in COX-2 -1195 and the risk of endometriosis and adenomyosis

Yujie Wang, Y Wang, Yan Qu, Y Qu, Wei Song, W Song
Clinical and experimental obstetrics & gynecology · 2015 · vol. 42(2) , pp. 168–172 · doi:10.12891/ceog1747.2015 · PMID:26054111 · W1474541069
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that the G to A genetic variation at the COX-2 -1195 locus increases the risk for endometriosis and adenomyosis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This paper studied whether COX-2 promoter polymorphism at the -1195 (G to A) locus is associated with hereditary susceptibility to endometriosis and adenomyosis. Using genotyping in 170 endometriosis cases, 150 adenomyosis cases, and 240 matched controls without either condition, the authors found that GG/AG/AA genotype frequencies in both endometriosis and adenomyosis groups differed significantly from controls (p < 0.05), with higher A allele frequencies in cases. Individuals carrying two A alleles had increased risk compared with non-A genotypes, with risk estimates of 2.19 for endometriosis and 2.41 for adenomyosis. The paper notes that genetic susceptibility appears similar across both conditions, but it does not describe any additional limitation such as replication or functional validation. This paper is centrally about endometriosis and adenomyosis—specifically the association between COX-2 -1195 (G/A) polymorphism and increased risk for both diseases.

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Abstract

AIM: Ths study aims to explore the relationship between COX-2 gene polymorphism and the hereditary susceptibility or endoomeyriosis and adenomyosis. MATERIALS AND METHODS: Gene polymorphism in COX-2 gene was genotyped in 170 cases of endometriosis, 150 cases of adenomyosis, and 240 matched non-endometriosis and non-adenomyosis controls. RESULTS: Genotypic frequencies of GG, AG, and AA in COX-2 locus in endometriosis and adenomyosis were 16.5%, 51.2%, 32.4% and 16.0%, 49.3%, 34.7%, respectively. They were both significantly different from those in the control group (24.6%, 53.3%, and 22.1%) (p < 0.05). An allele frequency in endometriosis and adenomyosis were significantly higher than that in the control group. The risk of endometriosis or adenomyosis for those carrying two A alleles were 2.19 and 2.41 times to non-A genotype. CONCLUSION: Genetic variation of G to A at -1195 locus in the promoter region of COX-2 gene increases the risk of endometriosis and adenomyosis, and the genetic susceptibility of these two diseases are similar.
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Abstract

Aim: This study aims to explore the relationship between COX-2 gene polymorphism and the hereditary susceptibility of endometriosisand adenomyosis. Materials and Methods: Gene polymorphism in COX-2 gene was genotyped in 170 cases of endometriosis, 150 cases of adenomyosis, and 240 matched non-endometriosis and non-adenomyosis controls. Results: Genotypic frequencies of GG, AG, and AA in COX-2 locus in endometriosis and adenomyosis were 16.5%, 51.2%, 32.4% and 16.0%, 49.3%, 34.7%, respectively. They were bothsignificantly different from those in the control group (24.6%, 53.3%, and 22.1%) (p < 0.05). An allele frequency in endometriosis andadenomyosis were significantly higher than that in the control group. The risk of endometriosis or adenomyosis for those carrying two Aalleles were 2.19 and 2.41 times to non-A genotype. Conclusion: Genetic variation of G to A at -1195 locus in the promoter region of COX-2 gene increases the risk of endometriosis and adenomyosis, and the genetic susceptibility of these two diseases are similar.

Keywords

- Endometriosis - Adenomyosis - COX-2 - genetic susceptibility - Single nucleotide polymorphisms (SNPs)

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Condition tags

mesh:D004715endometriosisadenomyosis

MeSH descriptors

Adenomyosis Cyclooxygenase 2 Endometriosis Adenomyosis Adult Case-Control Studies China Cyclooxygenase 2 Endometriosis Female Gene Frequency Genetic Predisposition to Disease Genotype Humans Polymorphism, Genetic Polymorphism, Restriction Fragment Length Polymorphism, Single Nucleotide Promoter Regions, Genetic Risk

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